Using an Emotion Regulation Framework to Understand the Role of Temperament and Family Processes in Risk for Adolescent Depressive Disorders

Although recent evidence implicates the importance of the family for understanding depressive disorders during adolescence, we still lack a coherent framework for understanding the way in which the myriad of developmental changes occurring within early adolescents and their family environments actually operate to increase adolescents’ vulnerability to, or to protect them from, the development of depressive disorders. In this review we propose a framework that places the mechanisms and processes of emotion regulation at the centre of these questions. We argue that emotion regulation can provide an organising rubric under which the role of various factors, such as adolescent and parent temperament and emotion regulation, and parental socialization of child emotion, as well as the interaction amongst these factors, can be understood to account for the role of the family in adolescents’ risk for depression. In particular, we posit that adolescent emotion regulation functions as a mechanism through which temperament and family processes interact to increase vulnerability to developing depression.     

The Default Mode Network and Recurrent Depression: A Neurobiological Model of Cognitive Risk Factors

A neurobiological account of cognitive vulnerability for recurrent depression is presented based on recent developments of resting state neural networks. We propose that alterations in the interplay between task positive (TP) and task negative (TN) elements of the Default Mode Network (DMN) act as a neurobiological risk factor for recurrent depression mediated by cognitive mechanisms. In the framework, depression is characterized by an imbalance between TN-TP components leading to an overpowering of TP by TN activity. The TN-TP imbalance is associated with a dysfunctional internally-focused cognitive style as well as a failure to attenuate TN activity in the transition from rest to task. Thus we propose the TN-TP imbalance as overarching neural mechanism involved in crucial cognitive risk factors for recurrent depression, namely rumination, impaired attentional control, and cognitive reactivity. During remission the TN-TP imbalance persists predisposing to vulnerability of recurrent depression. Empirical data to support this model is reviewed. Finally, we specify how this framework can guide future research efforts.     

Role of Parenting and Maltreatment Histories in Unipolar and Bipolar Mood Disorders: Mediation by Cognitive Vulnerability to Depression

In this article, we review empirical research on the role of individuals' parenting and maltreatment histories as developmental antecedents for symptoms and diagnosable episodes of unipolar and bipolar spectrum disorders. Our review is focused on the following three overarching questions: (1) Do negative parenting and a history of maltreatment contribute risk to symptoms or diagnosable episodes of unipolar and bipolar disorders? (2) Are the associations of negative parenting and maltreatment histories with bipolar disorders similar to those for unipolar depression? and (3) Are the associations between negative parenting and maltreatment histories and unipolar and bipolar symptoms or disorders mediated by cognitive vulnerability to depression? We begin by discussing the methodological requirements for demonstrating a psychosocial risk factor and the methodological issues that plague the parenting and maltreatment literatures. Next, we review the extant studies on the role of parenting histories in unipolar and bipolar disorders. We consider the specificity and possible moderators of the parenting-mood disorder relationship, as well as cognitive vulnerability to depression as a mediator of this relationship. Then, we review studies on the association of maltreatment histories with unipolar and bipolar disorders and the role of cognitive vulnerability to depression as a mediator of this association. We conclude with an assessment of the state of the parenting and maltreatment literatures in unipolar and bipolar disorder with regard to our guiding questions.     

Cognitive Vulnerabilities as Mediators between Emotional Abuse and Depressive Symptoms

This study tested whether childhood parental emotional abuse and peer emotional bullying serve as antecedents of depression in adolescence and identified the cognitive mechanisms involved in this process. It was hypothesized that the experience of emotional abuse would predict depressive symptoms via development of rumination and negative inferences. A 3-wave longitudinal study was carried out with 998 adolescents (471 girls and 526 boys) between 13 and 17 years of age. Results showed that emotional abuse by parents and peers at Time 1 predicted a worsening of several cognitive vulnerabilities at Time 2. In addition, brooding mediated between the experiences of abuse and the increase of depressive symptoms at Time 3. Thus, findings suggest that the experiences of childhood emotional abuse by parents and peers serve as antecedents to develop a negative cognitive style, vulnerability that, once developed, is a risk factor for the onset of depressive symptoms in adolescence.     

A review of cognitive biases in youth depression: attention,interpretation and memory

Depression is one of the most common mental health problems in childhood and adolescence. Although data consistently show it is associated with self-reported negative cognitive styles, less is known about the mechanisms underlying this relationship. Cognitive biases in attention, interpretation and memory represent plausible mechanisms and are known to characterise adult depression. We provide the first structured review of studies investigating the nature and causal role of cognitive biases in youth depression. Key questions are (i) do cognitive biases characterise youth depression? (ii) are cognitive biases a vulnerability factor for youth depression? and (iii) do cognitive biases play a causal role in youth depression? We find consistent evidence for positive associations between attention and interpretation biases and youth depression. Stronger biases in youth with an elevated risk of depression support cognitive-vulnerability models. Preliminary evidence from cognitive bias modification paradigms supports a causal role of attention and interpretation biases in youth depression but these paradigms require testing in clinical samples before they can be considered treatment tools. Studies of memory biases in youth samples have produced mixed findings and none have investigated the causal role of memory bias. We identify numerous areas for future research in this emerging field.     

Neuroticism,Life Events and Negative Thoughts in the Development of Depression in Adolescent Girls

Theories of depression suggest that cognitive and environmental factors may explain the relationship between personality and depression. This study tested such a model in early adolescence, incorporating neuroticism, stress-generation and negative automatic thoughts in the development of depressive symptoms. Participants (896 girls, mean age 12.3 years) completed measures of personality and depressive symptoms, and 12 months later completed measures of depressive symptoms, recent stressors and negative automatic thoughts. Path analysis supported a model in which neuroticism serves as a distal vulnerability for depression, conferring a risk of experiencing dependent negative events and negative automatic thoughts, which fully mediate the effect of neuroticism on later depression. A second path supported a maintenance model for depression in adolescence, with initial levels of depression predicting dependent negative events, negative automatic thoughts and subsequent depressive symptoms. Unexpectedly, initial depression was also associated with later independent life events. This study establishes potential mechanisms through which personality contributes to the development of depression in adolescent girls.     

Do Negative Cognitive Styles Confer Vulnerability to Depression?

According to the cognitive-vulnerability hypothesis of depression, negative cognitive styles confer vulnerability to depression when people confront negative life events. In this article, we present evidence that negative cognitive styles do indeed confer vulnerability to clinically significant depressive disorders and suicidality and discuss possible developmental antecedents of cognitive vulnerability to depression. We consider the issue of stability versus change in cognitive vulnerability to depression and discuss the broader implications of the cognitive-vulnerability findings for mental and physical health.     

Understanding vulnerability for depression from a cognitive neuroscience perspective: A reappraisal of attentional factors and a new conceptual framework

We propose a framework to understand increases in vulnerability for depression after recurrent episodes that links attention processes and schema activation to negative mood states, by integrating cognitive and neurobiological findings. Depression is characterized by a mood-congruent attentional bias at later stages of information processing. The basic idea of our framework is that decreased activity in prefrontal areas, mediated by the serotonin metabolism which the HPA axis controls, is associated with an impaired attenuation of subcortical regions, resulting in prolonged activation of the amygdala in response to stressors in the environment. Reduced prefrontal control in interaction with depressogenic schemas leads to impaired ability to exert attentional inhibitory control over negative elaborative processes such as rumination, leading in turn to sustained negative affect. These elaborative processes are triggered by the activation of negative schemas after confrontation with stressors. In our framework, attentional impairments are postulated as a crucial process in explaining the increasing vulnerability after depressive episodes, linking cognitive and biological vulnerability factors. We review the empirical data on the biological factors associated with the attentional impairments and detail how they are associated with rumination and mood regulation. The aim of our framework is to stimulate translational research.     

Early Health Risk Factors for Violence: Conceptualization, Review of the Evidence, and Implications

Violence and aggression are public health problems that can benefit from ongoing research into risk reduction and prevention. Current developmental theories of violence and aggression emphasize biological and psychosocial factors, particularly during adolescence. However, there has been less focus on understanding the interactive, multiplicative effects of these processes. Furthermore, little attention has been given to the pre-, peri-, and postnatal periods, where prevention and intervention may yield effective results. Early health risk factors that influence negative behavioral outcomes include prenatal and postnatal nutrition, tobacco use during pregnancy, maternal depression, birth complications, traumatic brain injury, lead exposure, and child abuse. There is an ample literature to suggest that these early health risk factors may increase the likelihood of childhood externalizing behaviors, aggression, juvenile delinquency, adult criminal behavior, and/or violence. This paper proposes an early health risk factors framework for violence prediction, built on existing developmental theories of criminal behavior and supported by empirical findings. This framework addresses gaps in the adolescent psychopathology literature and presents a novel conceptualization of behavioral disturbance that emphasizes the pre-, peri-, and post-natal periods, when a child's development is critical and the opportunity for behavioral and environmental modification is high. Implications for such a framework on violence prevention programs are discussed.     

Examining the link between adolescent brain development and risk taking from a social–developmental perspective

The adolescent age period is often characterized as a health paradox because it is a time of extensive increases in physical and mental capabilities, yet overall mortality/morbidity rates increase significantly from childhood to adolescence, often due to preventable causes such as risk taking. Asynchrony in developmental time courses between the affective/approach and cognitive control brain systems, as well as the ongoing maturation of neural connectivity are thought to lead to increased vulnerability for risk taking in adolescence. A critical analysis of the frequency of risk taking behaviors, as well as mortality and morbidity rates across the lifespan, however, challenges the hypothesis that the peak of risk taking occurs in middle adolescence when the asynchrony between the different developmental time courses of the affective/approach and cognitive control systems is the largest. In fact, the highest levels of risk taking behaviors, such as alcohol and drug use, often occur among emerging adults (e.g., university/college students), and highlight the role of the social context in predicting risk taking behavior. Moreover, risk taking is not always unregulated or impulsive. Future research should broaden the scope of risk taking to include risks that are relevant to older adults, such as risky financial investing, gambling, and marital infidelity. In addition, a lifespan perspective, with a focus on how associations between neural systems and behavior are moderated by context and trait-level characteristics, and which includes diverse samples (e.g., divorced individuals), will help to address some important limitations in the adolescent brain development and risk taking literature.     

Examining the link between adolescent brain development and risk taking from a social–developmental perspective (reprinted)

The adolescent age period is often characterized as a health paradox because it is a time of extensive increases in physical and mental capabilities, yet overall mortality/morbidity rates increase significantly from childhood to adolescence, often due to preventable causes such as risk taking. Asynchrony in developmental time courses between the affective/approach and cognitive control brain systems, as well as the ongoing maturation of neural connectivity are thought to lead to increased vulnerability for risk taking in adolescence. A critical analysis of the frequency of risk taking behaviors, as well as mortality and morbidity rates across the lifespan, however, challenges the hypothesis that the peak of risk taking occurs in middle adolescence when the asynchrony between the different developmental time courses of the affective/approach and cognitive control systems is the largest. In fact, the highest levels of risk taking behaviors, such as alcohol and drug use, often occur among emerging adults (e.g., university/college students), and highlight the role of the social context in predicting risk taking behavior. Moreover, risk taking is not always unregulated or impulsive. Future research should broaden the scope of risk taking to include risks that are relevant to older adults, such as risky financial investing, gambling, and marital infidelity. In addition, a lifespan perspective, with a focus on how associations between neural systems and behavior are moderated by context and trait-level characteristics, and which includes diverse samples (e.g., divorced individuals), will help to address some important limitations in the adolescent brain development and risk taking literature.     

Differentiating Adolescent Self-Injury from Adolescent Depression: Possible Implications for Borderline Personality Development

Self-inflicted injury (SII) in adolescence marks heightened risk for suicide attempts, completed suicide, and adult psychopathology. Although several studies have revealed elevated rates of depression among adolescents who self injure, no one has compared adolescent self injury with adolescent depression on biological, self-, and informant-report markers of vulnerability and risk. Such a comparison may have important implications for treatment, prevention, and developmental models of self injury and borderline personality disorder. We used a multi-method, multi-informant approach to examine how adolescent SII differs from adolescent depression. Self-injuring, depressed, and typical adolescent females (n = 25 per group) and their mothers completed measures of psychopathology and emotion regulation, among others. In addition, we assessed electrodermal responding (EDR), a peripheral biomarker of trait impulsivity. Participants in the SII group (a) scored higher than depressed adolescents on measures of both externalizing psychopathology and emotion dysregulation, and (b) exhibited attenuated EDR, similar to patterns observed among impulsive, externalizing males. Self-injuring adolescents also scored higher on measures of borderline pathology. These findings reveal a coherent pattern of differences between self-injuring and depressed adolescent girls, consistent with theories that SII differs from depression in etiology and developmental course.     

A Latent Structure Analysis of Cognitive Vulnerability to Depression in Adolescence

Whether cognitive vulnerability to depression exists along a continuum of severity or as a qualitatively discrete phenomenological entity has direct bearing on theoretical formulations of risk for depression and clinical risk assessment. This question is of particular relevance to adolescence, given that cognitive vulnerability appears to coalesce and rates of depression begin to rise markedly during this period of development. Although a dimensional view is often assumed, it is necessary to submit this assumption to direct empirical evaluation. Taxometric analysis is a family of statistical techniques developed directly to test such assumptions. The present study applied taxometric methods to address this question in a community sample of early adolescents (n = 485), drawing on three indices of cognitive vulnerability to depression (i.e., negative inferential style, ruminative response style, self-referent information processing). The results of three taxometric analyses (i.e., mean above minus below a cut [MAMBAC], maximum eigenvalue [MAXEIG], and latent mode [L-Mode]) were consistent in unambiguously supporting a dimensional conceptualization of this construct. The latent structure of the tested indices of cognitive vulnerability to depression in adolescence appears to exist along a continuum of severity rather than as a discrete clinical entity.     

A social neuroscience perspective on adolescent risk-taking

This article proposes a framework for theory and research on risk-taking that is informed by developmental neuroscience. Two fundamental questions motivate this review. First, why does risk-taking increase between childhood and adolescence? Second, why does risk-taking decline between adolescence and adulthood? Risk-taking increases between childhood and adolescence as a result of changes around the time of puberty in the brain’s socio-emotional system leading to increased reward-seeking, especially in the presence of peers, fueled mainly by a dramatic remodeling of the brain’s dopaminergic system. Risk-taking declines between adolescence and adulthood because of changes in the brain’s cognitive control system—changes which improve individuals’ capacity for self-regulation. These changes occur across adolescence and young adulthood and are seen in structural and functional changes within the prefrontal cortex and its connections to other brain regions. The differing timetables of these changes make mid-adolescence a time of heightened vulnerability to risky and reckless behavior.     

The ABCs of depression: integrating affective, biological, and cognitive models to explain the emergence of the gender difference in depression

In adulthood, twice as many women as men are depressed, a pattern that holds in most nations. In childhood, girls are no more depressed than boys, but more girls than boys are depressed by ages 13 to 15. Although many influences on this emergent gender difference in depression have been proposed, a truly integrated, developmental model is lacking. The authors propose a model that integrates affective (emotional reactivity), biological (genetic vulnerability, pubertal hormones, pubertal timing and development) and cognitive (cognitive style, objectified body consciousness, rumination) factors as vulnerabilities to depression that, in interaction with negative life events, heighten girls' rates of depression beginning in adolescence and account for the gender difference in depression.     

Depressogenic cognitive styles: predictive validity, information processing and personality characteristics, and developmental origins.

Two of the major cognitive theories of depression, the theory of Beck [Beck, A. T. (1967). Depression: clinical, experimental and theoretical aspects. New York: Harper & Row. and Beck, A. T. (1987) Cognitive models of depression. Journal of Cognitive Psychotherapy: an International Quarterly, 1, 5-37] and the hopelessness theory [Abramson, Metalsky, & Alloy, (1989) Hopelessness depression: a theory-based subtype of depression. Psychological Review, 96, 358-372], include the hypothesis that particular negative cognitive styles increase individuals' likelihood of developing episodes of depression, in particular, a cognitively mediated subtype of depression, when they encounter negative life events. The Temple-Wisconsin Cognitive Vulnerability to Depression (CVD) project is a two-site, prospective longitudinal study designed to test this cognitive vulnerability hypothesis, as well as the other etiological hypotheses of Beck's and the hopelessness theories of depression. In this article, based on CVD project findings to date, we review evidence that the hypothesized depressogenic cognitive styles do indeed confer vulnerability for clinically significant depressive disorders and suicidality. In addition, we present evidence regarding moderators of these depressogenic cognitive styles, the information processing and personality correlates of these styles and the possible developmental antecedents of these styles. We end with a consideration of future research directions and the clinical implications of cognitive vulnerability to depression.     

A Review of Preclinical Studies to Understand Fear During Adolescence

The most rapid physical and psychological growth occurs during adolescence, a period of transition from childhood to adulthood when the incidence of anxiety disorder peaks in humans. Human and animal studies suggest that dramatic changes in prefrontal cortical areas during adolescence are responsible for such prevalence of anxiety. Only recently, however, has the relationship between prefrontal immaturity and differential fear processing across adolescence been directly and systematically examined. Such progress is largely due to the culmination of rodent studies that delineated the fear learning, expression, and inhibition neural circuitry, and preclinical studies that provided avenues for translation. This article summarises those initial findings on the circuitry of fear inhibition, and describes in detail the new findings on adolescent fear inhibition that highlight the prefrontal cortex as a key, unrefined brain region that may govern adolescent vulnerability to anxiety disorders. Specifically, adolescent rodents have been demonstrated to be impaired in inhibiting learned fear responses following fear extinction due to prefrontal immaturity, a discovery that was shortly after replicated in adolescent humans (at least the behavioural component). Our desire for this article is to acquaint both research and clinical psychologists with the neural circuitry of fear learning and extinction, turn the attention to developmental work, and facilitate translation of preclinical rodent findings in humans.     

When interventions harm. Peer groups and problem behavior.

This article explored developmental and intervention evidence relevant to iatrogenic effects in peer-group interventions. Longitudinal research revealed that "deviancy training" within adolescent friendships predicts increases in delinquency, substance use, violence, and adult maladjustment. Moreover, findings from 2 experimentally controlled intervention studies suggested that peer-group interventions increase adolescent problem behavior and negative life outcomes in adulthood, compared with control youth. The data from both experimental studies suggested that high-risk youth are particularly vulnerable to peer aggregations, compared with low-risk youth. We proposed that peer aggregation during early adolescence, under some circumstances, inadvertently reinforces problem behavior. Two developmental processes are discussed that might account for the powerful iatrogenic effects.     

Cognitive and Interpersonal Vulnerabilities to Adolescent Depression: Classification of Risk Profiles for a Personalized Prevention Approach

Despite interest in psychosocial vulnerabilities to depression, little is known about reliable and valid individualized risk profiles that can be used to match individuals to evidence-based interventions for depression. This study investigated well-established cognitive and interpersonal vulnerabilities to depression among youth to discern an evidence-based risk classification approach which is being used in a personalized depression prevention randomized clinical trial. Data were drawn from a general community sample of adolescents (N?=?467; ages 10–16, mean 13.14, SD?=?1.62; 57% females) who were followed prospectively for 3 years. Youth completed measures of cognitive (negative cognitive style, dysfunctional attitudes, rumination) and interpersonal (support and conflict with peers and parents, excessive reassurance seeking, social competence, co-rumination) risks to depression, and then were followed longitudinally for onset of depression. Principal axis factor analyses showed that three latent factors--cognitive vulnerability, interpersonal support, and interpersonal conflict--optimally represented the structure of these risk factors. Clinically practical and meaningful cutoffs, based on tertile cut-off scores on cognitive and interpersonal risk measures, were used to categorize youth into relatively balanced high and low cognitive and interpersonal risk groups. These risk classification groups exhibited validity (AUC?>?0.70) by predicting prospective onsets of depressive episodes at 18-months follow-ups. These findings demonstrate a reliable and valid approach to synthesize psychosocial vulnerabilities to depression, specifically cognitive and interpersonal risks. Results are discussed in terms of using these risk classifications profiles to test personalized prevention of depression during adolescence.     

Risk Factors for Disordered Eating During Early and Middle Adolescence: A Two Year Longitudinal Study of Mainland Chinese Boys and Girls

Even though reliable eating disorder risk factors have been identified among adolescent girls, little is known about predictors of increased vulnerability within specific phases of adolescence or among adolescent boys, particularly in highly populated non-Western contexts. In this study, early and middle adolescent boys (n?=?1,271) and girls (n?=?1,415) from Chongqing, China completed validated measures of eating disorder pathology and putative risk factors at baseline and 2 years follow-up. Multivariate models for boys of each age group indicated increases in disordered eating at follow-up were predicted by higher initial body mass index, negative affect and body dissatisfaction levels as well as attendant increases in perceived appearance pressure from mass media, body dissatisfaction, negative affect between assessments. High baseline levels of reported appearance pressure from parents and dating partners contributed, respectively, to prediction models of younger and older boys. More distinct constellations of significant predictors emerged in multivariate models of early versus middle adolescent girls. Together, findings indicated body dissatisfaction and negative affect were fairly robust risk factors for exacerbations in disturbances across samples while risk factors such as perceived pressure from desired/prospective dating partners were salient only during particular phases of adolescence.